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Summary
The name carnitine is derived from the Latin "carnus" or flesh, as the compound was first isolated from meat.
Carnitine is termed a conditionally essential nutrient, as under certain conditions its requirements may exceed
the individual's capacity to synthesize it. Carnitine mediates the transport of medium/long-chain fatty acids
across mitochondrial membranes, facilitating their oxidation with subsequent energy production; in addition, it
facilitates the transport of intermediate toxic compounds out of the mitochondria preventing their
accumulation. Because of these key functions, carnitine is concentrated in tissues that utilize fatty acids as
their primary dietary fuel, such as skeletal and cardiac (heart) muscle. Dietary sources of carnitine include
foods of animal origin, such as meat and dairy products. In general, healthy adults do not require dietary
carnitine as carnitine stores are replenished through endogenous synthesis from lysine and methionine in the
liver and kidneys. Excess carnitine is excreted via the kidneys. In the US, carnitine is an approved prescription
drug for the treatment of primary systemic carnitine deficiency and secondary carnitine deficiency syndromes.
Carnitine is also available over-the-counter as a dietary supplement, as an aid to weight loss, to improve
exercise performance, and to enhance a sense of well-being.
Carnitine is the generic term for a number of compounds that include L-carnitine, L-acetylcarnitine, acetyl-Lcarnitine, and L-propionyl carnitine. The only forms available over-the-counter in the US are L-carnitine and
acetyl-L-carnitine. L-carnitine is the biological active form. The D-isomer, which is not biologically active,
can compete with the L-isomer potentially increasing the risk of L-carnitine deficiency. Proprionyl-L-carnitine
is approved for use in Europe but not in the US.
Carnitine is studied extensively in part because of the important role it plays in fatty acid oxidation and energy
production, and because it is a well-tolerated and generally safe therapeutic agent. It is proven treatment in
children who have recessive defects in the carnitine transporter system and in individuals treated with pivalate
containing antibiotics. Other benefits attributed to carnitine result from the management of secondary carnitine
deficiencies. These benefits are supported by preliminary findings and need to be confirmed through wellcontrolled randomized trials. While there is agreement on carnitine's role as a prescription product for the
treatment of primary carnitine deficiencies, its benefits as a dietary supplement in individuals who are
carnitine sufficient is debated.
L-CARNITINE
L-Carnitine is a derivative of the amino acid, lysine. Its name is derived from the fact that it was first isolated
from meat (carnus) in 1905. Because L-carnitine appeared to act as a vitamin in the mealworm (Tenebrio
molitor), it was called vitamin BT. Vitamin BT turned out to be a misnomer when scientists discovered that
humans and other higher organisms synthesize L-carnitine. Under certain conditions, the demand for Lcarnitine may exceed an individual's capacity to synthesize it, making it a conditionally essential nutrient (1).
FUNCTION
L-Carnitine is synthesized primarily in the liver and also in the kidneys, and must be transported to other
tissues. It is most concentrated in tissues that use fatty acids as their primary dietary fuel, such as skeletal and
cardiac (heart) muscle. In this regard, L-carnitine plays an important role in energy production by chaperoning
activated fatty acids (acyl-CoA) into the mitochondrial matrix for metabolism and chaperoning intermediate
compounds out of the mitochondrial matrix to prevent their accumulation.
Transport of long-chain fatty acids into the mitochondrial matrix
The transport of long-chain fatty acids by L-carnitine into the mitochondrial matrix where they can be
metabolized to generate energy requires three enzymes located on the mitochondrial outer and inner
membranes (diagram). On the outer mitochondrial membrane of skeletal and cardiac muscle cells, carnitinepalmitoyl transferase I (CPTI) catalyzes the formation of acylcarnitine (a fatty acid + L-carnitine) from acylCoA (a fatty acid + coenzyme A). A transporter protein called carnitine:acylcarnitine translocase (CT)
transports acylcarnitine across the inner mitochondrial membrane. Carnitine-palmitoyl transferase II (CPTII)
is associated with the inner mitochondrial membrane and catalyzes the formation of acyl-CoA within the
mitochondrial matrix where it can be metabolized through a process called beta-oxidation, ultimately yielding
propionyl-CoA and acetyl-CoA (2, 3).
Regulation of energy metabolism through the modulation of acetyl CoA:CoA ratios
The enzyme, pyruvate dehydrogenase (PDH), catalyzes the conversion of pyruvate to acetyl CoA, a pivotal
reaction in glucose metabolism. In the mitochondrial matrix, decreased free CoA, relative to acetyl CoA,
inhibits the activity of PDH. Carnitine acetyl-transferase (CAT) catalyzes the transfer of the acetyl group from
acetyl CoA to L-carnitine, freeing CoA to participate in the PDH reaction (diagram). Acetyl-L-carnitine can
be exported from the mitochondria through the activity of CT (2, 3).
Removal of short- and medium-chain fatty acids from the mitochondria
Within the mitochondrial matrix, short- and medium-chain fatty acids can be transferred from CoA to Lcarnitine, allowing short and medium-chain acyl-carnitines to be exported from the mitochondria. This
process provides free CoA needed for energy metabolism, as well as a mechanism to export excess acetyl and
acyl groups from the mitochondria. This mechanism may also play a role in the depletion of L-carnitine
during the metabolism of certain drugs (see Drug Interactions) (2).
DEFICIENCY
Primary carnitine deficiencies
The primary carnitine deficiencies, systemic carnitine deficiency and myopathic carnitine deficiency, are
relatively rare hereditary disorders.
Systemic carnitine deficiency: Primary systemic carnitine deficiency is a genetic disorder that is usually
detected in infancy or early childhood. It is characterized by low serum L-carnitine levels, and if untreated
may result in life-threatening damage to the liver, heart, or brain. Also known as carnitine carrier deficiency,
the underlying cause is a mutation in the gene coding for the protein that transports L-carnitine into cells. As a
result of this defect, intestinal absorption of dietary L-carnitine is poor and reabsorption by the kidney is
impaired, resulting in increased urinary loss of L-carnitine (1).
Myopathic carnitine deficiency: Primary myopathic carnitine deficiency is also a genetic disorder in which
carnitine deficiency is limited to skeletal and cardiac muscle. Serum L-carnitine levels are generally normal.
The symptoms of myopathic carnitine deficiency include muscle pain and progressive muscle weakness.
Symptoms may begin in childhood or adulthood. The myopathic form of primary carnitine deficiency is
generally less severe than the systemic form (1).
Secondary carnitine deficiencies
Secondary carnitine deficiencies may be hereditary or acquired. In all cases, they are characterized by
decreased availability of free L-carnitine. In such cases, total L-carnitine levels may be normal, but free Lcarnitine levels are decreased.
Hereditary causes: Hereditary causes of secondary carnitine deficiency include genetic defects in amino acid
degradation (e.g., propionic aciduria) and lipid metabolism (e.g., medium chain acyl-CoA dehydrogenase
deficiency).
Increased L-carnitine loss: Hemodialysis (see Disease Treatment), Fanconi syndrome, and the metabolism
of some medications (see Drug Interactions) may result in substantial L-carnitine loss, resulting in L-carnitine
deficiency (1).
Insufficient L-carnitine synthesis: Malabsorption syndromes and diets that chronically lack L-carnitine and
its precursors (see Nutrient interactions) may increase the risk of secondary carnitine deficiency. Premature
infants may be at risk of secondary L-carnitine deficiency when fed soy-based formulas without added Lcarnitine. Therefore, it is recommended that non-milk based infant formulas be fortified with the amount of Lcarnitine normally found in human milk (11 mg/liter). Although dietary L-carnitine comes mainly from
animal sources, even strict vegetarians can generally synthesize enough L-carnitine to prevent deficiency (3).
Nutrient interactions
The synthesis of L-carnitine is catalyzed by the concerted action of five different enzymes. This process
requires two essential amino acids (lysine and methionine), iron (Fe2+), vitamin C, vitamin B6, and niacin in
the form of nicotinamide adenine dinucleotide (NAD) (1). One of the earliest symptoms of vitamin C
deficiency is fatigue, thought to be related to decreased synthesis of L-carnitine (4).
SOURCES
Biosynthesis
The normal rate of L-carnitine biosynthesis in humans ranges from 0.16 to 0.48 mg/kg of body weight/day
(1). Thus, a 70 kg (154 1b) person would synthesize from 11 to 34 mg/day. This rate of synthesis combined
with the reabsorption of about 95% of the L-carnitine filtered by the kidneys is enough to prevent deficiency
in generally healthy people, including strict vegetarians (3).
Food sources
Meat, poultry, fish, and dairy products are the richest sources of L-carnitine. Tempeh (fermented soybeans),
wheat, and avocados contain some L-carnitine, while fruits, vegetables, and grains contain relatively little Lcarnitine to the diet. Omnivorous diets have been found to provide 20 to 200 mg/day of L-carnitine for a 70 kg
person, while strict vegetarian diets may provide as little as 1 mg/day for a 70 kg person. Between 63% and
75% of L-carnitine from food is absorbed, compared to 15%-20% from oral supplements (3, 5). Non-milk
based infant formulas (e.g., soy formulas) should be fortified so that they contain 11 mg/liter. Some carnitinerich foods and their carnitine content in milligrams (mg) are listed in the table below (3).
Food
Serving
L-Carnitine (mg)
Beef steak
3 ounces*
81
Ground beef
3 ounces
80
Pork
3 ounces
24
Canadian bacon
3 ounces
20
Milk (whole)
8 fluid ounces (1 cup) 8
Fish (cod)
3 ounces
5
Chicken breast
3 ounces
3
Ice cream
4 ounces (1/2 cup)
3
Avocado
1 medium
2
American cheese
1 ounce
1
Whole-wheat bread
2 slices
0.2
Asparagus
6 spears (1/2 cup)
0.2
*A 3-ounce serving of meat is about the size of a deck of cards.
Supplements
Intravenous L-carnitine is available by prescription only for the treatment of primary and secondary Lcarnitine deficiencies.
Oral L-carnitine is available by prescription for the treatment of primary and secondary L-carnitine
deficiencies. It is also available without a prescription as a nutritional supplement. Supplemental doses usually
range from 500 mg to 2,000 mg/day.
Acetyl-L-carnitine is available without a prescription as a nutritional supplement. In addition to providing Lcarnitine, it provides acetyl groups, which may be used in the formation of the neurotransmitter, acetylcholine.
Supplemental doses usually range from 500 mg to 2,000 mg/day (6).
Propionyl-L-carnitine is available in Europe, but not the U.S. It provides L-carnitine as well as propionate,
which may be utilized as an intermediate during energy metabolism (5).
See a diagram of the chemical structures of L-carnitine, acetyl-L-carnitine, and propionyl-L-carnitine.
DISEASE PREVENTION
Aging
Age-related declines in mitochondrial function and increases in mitochondrial oxidant production are thought
to be important contributors to the adverse affects of aging. Tissue L-carnitine levels have been found to
decline with age in humans and animals (7). Feeding aged rats acetyl-L-carnitine (ALCAR) reversed agerelated declines in tissue L-carnitine levels and reversed a number of age-related changes in mitochondrial
function, but high doses of ALCAR increased liver mitochondrial oxidant production (8). More recently, a
series of studies in aged rats found that supplementation with either ALCAR or alpha-lipoic acid, a
mitochondrial cofactor and antioxidant, improved mitochondrial energy metabolism, decreased oxidative
stress, and improved memory (9, 10). Interestingly, supplementation with the combination of ALCAR and
alpha-lipoic acid resulted in significantly greater improvement than either compound alone. While these
findings are very exciting, the researchers involved caution that these studies used relatively high doses of the
compounds and only for a short time (one month). It is not yet known whether taking relatively high doses of
these two naturally occurring substances will benefit rats in the long-term or will have similar effects in
humans. Clinical trials in humans are planned, but it will be several years before the results are available.
For more information about aging and oxidative stress, see the article, Aging with Dr. Tory Hagen, in the
Fall/Winter 2000 Linus Pauling Institute Newsletter.
DISEASE TREATMENT
Conditions related to myocardial ischemia (insufficient blood supply to the heart muscle)
In the studies discussed below it is important to note that treatment with L-carnitine or propionyl-L-carnitine
was used as an adjunct (in addition) to appropriate medical therapy not in place of it.
Myocardial infarction (heart attack): Myocardial infarction (MI) occurs when atherosclerotic plaque in
a coronary artery ruptures. The resultant blood clot can obstruct the blood supply to the heart muscle,
causing in injury or damage to the heart. L-Carnitine treatment has been found to reduce injury to heart
muscle resulting from ischemia in several animal models (11). In humans, the administration of Lcarnitine immediately after the diagnosis of MI has resulted in improved clinical outcomes in several
small clinical trials. In one trial, half of 160 men and women diagnosed with a recent MI were randomly
assigned to receive 4 grams/day of L-carnitine in addition to standard pharmacological treatment. After
one year of treatment, mortality was significantly lower in the L-carnitine supplemented group (1.2% vs.
12.5%), and attacks of angina were less frequent (12). Not all clinical trials have found L-carnitine
supplementation to be beneficial after MI. In a randomized, double blind, placebo controlled trial, 60 men
and women diagnosed with an acute MI were treated with either intravenous L-carnitine (6 grams/day) for
7 days followed by oral L-carnitine (3 grams/day) for 3 months or placebo (13). After 3 months, mortality
did not differ between the 2 groups, nor did echocardiographic measures of cardiac function. In a larger
placebo-controlled trial, 472 patients treated in an intensive care unit within 24 hours of having their first
MI were randomly assigned to intravenous L-carnitine therapy (9 grams/day) for 5 days followed by oral
L-carnitine (6 grams/day) for 12 months or a placebo in addition to standard medical therapy (14, 15).
Although there were no significant differences in mortality or the incidence of congestive heart failure
(CHF), left ventricular volumes were significantly lower in the L-carnitine treated group at the end of one
year, suggesting that carnitine therapy may limit adverse effects of acute MI on the heart muscle. Based
on these findings, a randomized placebo-controlled trial in 4,000 patients with acute MI is planned to
determine the effect of L-carnitine therapy on the incidence of heart failure 6 months after MI (15).
Heart Failure: Impairment of the heart's ability to pump enough blood for all of the body's needs is
known as heart failure. In coronary artery disease, the accumulation of atherosclerotic plaque in the
coronary arteries may prevent parts of the heart muscle from getting adequate circulation, ultimately
resulting in damage and impaired pumping ability. Myocardial infarction (MI) may also damage the heart
muscle, resulting in the development of heart failure. Because physical exercise increases the demand on
the weakened heart, measures of exercise tolerance are frequently used to monitor the severity of heart
failure. Echocardiography is also used to determine the left ventricular ejection fraction (LVEF), an
objective measure of the heart's pumping ability. An LVEF of less than 40% is indicative of systolic heart
failure (16).
The addition of L-carnitine to standard medical therapy for heart failure has been evaluated in several
clinical trials. In a randomized, single-blind, placebo-controlled trial in 30 heart failure patients, oral
administration of 1.5 grams/day of propionyl-L-carnitine for 1 month resulted in significantly improved
measures of exercise tolerance and a slight but significant decrease in left ventricular size compared to
placebo (17). A larger randomized, double blind, placebo-controlled trial compared the addition of
propionyl-L-carnitine (1.5 grams/day) to the treatment regimen of 271 heart failure patients to a placebo
in 266 patients for 6 months (18). Overall, exercise tolerance was not different between the two groups.
However, in those with higher LVEF values (greater than 30%), exercise tolerance was significantly
improved in those taking propionyl-L-carnitine compared to placebo, suggesting that propionyl-Lcarnitine may help to improve exercise tolerance in higher functioning heart failure patients..
Angina pectoris: Angina pectoris is chest pain that occurs when the coronary blood supply is insufficient
to meet the metabolic needs of the heart muscle (ischemia). The addition of L-carnitine or propionyl-Lcarnitine to pharmacologic therapy for chronic stable angina has been found to modestly improve exercise
tolerance and decrease electrocardiographic signs of ischemia during exercise testing in a limited number
of angina patients. In a randomized, placebo-controlled crossover trial in 44 men with chronic stable
angina, 2 grams/day of L-carnitine for 4 weeks significantly increased the exercise workload tolerated
prior to the onset of angina and decreased ST segment depression (electrocardiographic evidence of
ischemia) during exercise compared to placebo (19). In a more recent randomized placebo-controlled trial
in 47 men and women with chronic stable angina, the addition of 2 grams/day of L-carnitine for 3 months
significantly improved exercise duration and decreased the time required for exercise-induced ST segment
changes to return to baseline compared to placebo (20).
Intermittent claudication in peripheral arterial disease
In peripheral arterial disease, atherosclerosis of the arteries supplying the lower extremities may diminish
blood flow to the point that it is insufficient to supply the metabolic needs of exercising muscles, leading to
ischemic leg or hip pain known as claudication (21). In a randomized placebo-controlled study of 495 patients
with intermittent claudication, 2 grams/day of propionyl-L-carnitine for 12 months significantly increased
maximal walking distance and the distance walked prior to the onset of claudication in patients whose initial
maximal walking distance was less than 250 meters (22). However, no significant response to propionyl-Lcarnitine treatment was observed in more mildly affected patients whose initial maximal walking distance was
greater than 250 meters. In a double blind, randomized, placebo-controlled trial of 155 patients with disabling
claudication in the U.S. and Russia, 2 grams/day of propionyl-L-carnitine for 6 months significantly improved
walking distance and claudication onset time compared to placebo. One study compared the efficacy of Lcarnitine and propionyl-L-carnitine administered intravenously for the treatment of intermittent claudication,
and concluded that propionyl-L-carnitine was more effective than L-carnitine when the same amount of
carnitine was provided (23).
Chronic renal failure/dialysis
L-Carnitine and many of its precursors are removed from the circulation during dialysis. Impaired L-carnitine
synthesis by the kidneys may also contribute to the potential for carnitine deficiency in patients with end-stage
renal failure on hemodialysis. The U.S. Food and Drug Administration (FDA) has approved the use of Lcarnitine in hemodialysis patients for the prevention and treatment of carnitine deficiency (24). Carnitine
depletion may lead to a number of conditions observed in dialysis patients, including muscle weakness and
fatigue, plasma lipid abnormalities, and refractory anemia. A systematic review that examined the results of
18 randomized trials, including a total of 482 dialysis patients, found that L-carnitine treatment was associated
with improved hemoglobin levels in studies performed before recombinant erythropoietin (EPO) was
routinely used to treat anemia in dialysis patients, and that L-carnitine treatment decreased EPO dose and
resistance to EPO in studies performed when patients routinely received EPO (25). Although some
uncontrolled studies found that L-carnitine treatment improved blood lipid profiles in hemodialysis patients
(26), the systematic review of randomized controlled trials did not find evidence that L-carnitine improved
lipid profiles (25). The National Kidney Foundation (NKF) does not recommend routine administration of Lcarnitine to all dialysis patients (27). However, the NKF and other consensus groups recommend a trial of Lcarnitine for maintenance hemodialysis patients with selected symptoms that do not respond to standard
therapy. Those symptoms include persistent muscle cramps or hypotension (low blood pressure) during
dialysis, severe fatigue, skeletal muscle weakness or myopathy, cardiomyopathy, and anemia requiring large
doses of EPO. In general, intravenous L-carnitine therapy (1-2 grams) at the end of a dialysis session has been
recommended for patients on hemodialysis. Oral administration of L-carnitine (1-3 grams/day in divided
doses) is more practical for patients on peritoneal dialysis (28).
Alzheimer's disease (dementia)
Several small controlled clinical trials conducted in the 1990's suggested that acetyl-L-carnitine (ALCAR)
treatment (2-3 g/day for 6-12 months) modestly slowed cognitive decline in patients with the clinical
diagnosis of Alzheimer's disease (29-31). However, a larger multicenter, randomized controlled trial involving
431 patients diagnosed with Alzheimer's disease did not find ALCAR treatment (3 grams/day for 12 months)
to be different than placebo in its effects on cognitive decline (32). Subsequent statistical analyses of that
study suggested that patients with early-onset Alzheimer's disease (65 years and younger) experienced more
rapid cognitive decline that was significantly slowed by ALCAR treatment (32, 33). More recently, a
multicenter, randomized controlled trial involving 229 early-onset Alzheimer's disease patients between 45
and 65 years of age did not find ALCAR treatment (3 grams/day for 12 months) to affect most measures of
cognitive decline with the exception of slightly decreased declines in attention compared to placebo (34).
HIV/AIDS
One of the hallmarks of infection with the retrovirus, HIV, is a progressive decline in the numbers of critical
immune cells known as CD4 T lymphocytes (CD4 cells), ultimately leading to the development of AIDS.
Lymphocytes of HIV-infected individuals inappropriately undergo programmed cell death (apoptosis).
Limited evidence in cell culture experiments and in humans suggests that L-carnitine supplementation may
help slow or prevent HIV-induced lymphocyte apoptosis. In an uncontrolled trial, 11 asymptomatic HIVinfected patients, who had refused antiretroviral treatment despite progressively declining CD4 cell counts,
were treated with 6 grams/day of L-carnitine intravenously for 4 months (35). After 4 months of L-carnitine
therapy, CD4 cell counts increased significantly and markers of lymphocyte apoptosis decreased, although
there was no significant change in plasma levels of the HIV virus (viremia). Long-term outcomes were not
reported in these patients. In a more recent study, 20 HIV-infected individuals were randomly assigned to
receive the antiretroviral agents, zidovudine (AZT) and didanosine (DDI), with or without supplemental Lcarnitine (36). Although CD4 cell counts and plasma HIV levels were not different between the two groups
after 7 months of therapy, indicators of CD4 cell apoptosis were significantly lower in the group taking Lcarnitine.
Some antiretroviral agents (nucleoside analogues) used to treat HIV-infection appear to cause a secondary Lcarnitine deficiency that may lead to some of their toxic side effects (see Drug interactions) (2). A small crosssectional study found that nerve concentrations of acetyl-L-carnitine were significantly lower in HIV patients
who developed peripheral neuropathy while taking nucleoside analogues than in control subjects (37). Ten out
of 16 HIV patients with painful neuropathies reported improvement after 3 weeks of intravenous or
intramuscular acetyl-L-carnitine treatment (38). Although more controlled research is needed before
conclusions can be drawn, L-carnitine supplementation may be a beneficial adjunct to antiretroviral therapy in
some HIV-infected individuals.
Decreased sperm motility
L-Carnitine is concentrated in the epididymis, where sperm mature and acquire their motility (39). Two
uncontrolled trials of L-carnitine supplementation in more than 100 men diagnosed with decreased sperm
motility in fertility clinics found that oral L-carnitine supplementation (3 grams/day) for 3 to 4 months
resulted in significantly improved sperm motility (40, 41). However, no information on subsequent fertility
was reported. A cross-sectional study of 101 fertile and infertile men found that L-carnitine concentrations in
semen were positively correlated with the number of sperm, the percentage of motile sperm, and the
percentage of normal appearing sperm in the sample (42), suggesting that measuring L-carnitine levels in
semen may be useful in the evaluation of male infertility. However, more controlled research on the effects of
L-carnitine on sperm motility is required before its utility in treating specific types of male infertility can be
determined.
PERFORMANCE
Athletic performance
Interest in the potential of L-carnitine supplementation to improve athletic performance is related to its
important roles in energy metabolism. In general, supplementing healthy people with oral L-carnitine for up to
3 months has not been found to result in significant improvements in athletic performance. However,
conclusions that can be drawn from this research are limited due to small numbers of participants, short
duration of supplementation, and lack of appropriate control groups in most studies (43, 44).
SAFETY
Toxicity
In general L-carnitine appears to be well tolerated. Toxic effects related to L-carnitine overdose have not been
reported. L-carnitine supplementation may cause mild gastrointestinal symptoms, including nausea, vomiting,
abdominal cramps and diarrhea. Supplements providing more than 3,000 mg/day may cause a "fishy" body
odor. Acetyl-L-carnitine has been reported to increase agitation in some Alzheimer's disease patients and to
increase seizure frequency and/or severity in some individuals with seizure disorders (6). Only the L-isomer of
carnitine is biologically active. The D-isomer may actually compete with L-carnitine for absorption and
transport, increasing the risk of L-carnitine deficiency (1). Supplements containing a mixture of the D-, and Lisomers (D,L-carnitine) were associated with muscle weakness in patients with kidney disease. Controlled
studies examining the safety of L-carnitine supplementation in pregnant and breastfeeding women are lacking
(6).
Drug Interactions
The anticonvulsant, valproic acid, and nucleoside analogues, used in the treatment of HIV infection, including
zidovudine (AZT), didanosine (ddI), zalcitabine (ddC) and stavudine (d4T), may produce secondary L-
carnitine deficiencies. Pivalic acid-containing antibiotics used in Europe (pivampicillin, pivmecillinam and
pivcephalexin) may also produce secondary L-carnitine deficiencies (3, 6). The cancer chemotherapy agents,
ifosfamide and cisplatin, may increase the risk of secondary L-carnitine deficiency, and there is limited
evidence that L-carnitine supplementation may help prevent cardiomyopathy induced by doxorubicin
(adriamycin) therapy (2).
SUMMARY
 L-Carnitine supplementation is indicated for the treatment of primary and secondary carnitine
deficiencies. More information
 Healthy individuals, including strict vegetarians, generally synthesize enough L-carnitine to prevent
deficiency. More information
 Hemodialysis patients with selected symptoms that do not respond to standard therapy may benefit
from a trial of L-carnitine supplementation. More information
 L-Carnitine supplementation appears promising as a treatment for intermittent claudication. More
information
 The roles of L-carnitine supplementation as an adjunct to standard medical therapy in myocardial
infarction, heart failure, angina pectoris, Alzheimer's disease, and HIV infection require further
research. More information
 Although recent studies in rats suggest acetyl-L-carnitine supplementation may be beneficial in
preventing age-related declines in energy metabolism and memory, it is not known whether acetyl-Lcarnitine supplementation will help prevent such age-related declines in humans. More information
 There is little evidence that L-carnitine supplementation improves athletic performance in healthy
people. More information
REFERENCES
L-CARNITINE REFERENCES
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RNA/DNA oxidation: partial reversal by feeding acetyl-L-carnitine and/or R-alpha -lipoic acid. Proc Natl
Acad Sci U S A. 2002;99(4):2356-2361. (PubMed)
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. ข้อมูลจาก
1. http://ods.od.nih.gov/News/Carnitine_Conference_Summary.aspx
2. http://lpi.oregonstate.edu/infocenter/othernuts/carnitine/